We demonstrated that imidacloprid self-poisoning resulted in mostly minor toxicity with a case-fatality of 0%. This is favourable compared to outcomes with other insecticides, in particular the widely used organophosphorus compounds which commonly have a case fatality between 5 and 30%. The most severely poisoned patients were both administered antidotes used for the treatment of organophosphorus pesticides and this may have increased the apparent toxicity. Many patients may have had a moderate metabolic acidosis on admission. Tachycardia and hypertension have usually been reported in previous cases, and recurrent ventricular fibrillation was the reported cause of death in a 69 year-old woman with coronary artery disease. Only 2 patients in our case series developed any cardiovascular toxicity which was predominantly hypotension and biomarkers of cardiac toxicity were not elevated. While electrocardiographic monitoring was not conducted in these patients, blood pressure improved with intravenous fluids. Therefore serious arrhythmias were unlikely to have caused the hypotension. Biochemical abnormalities and rhabdomyolysis have been reported as potentially serious complications that might lead to mortality. Most of the patients in our series had normal CK and biochemistry with the exception of low venous bicarbonate. The cause of this is not clear given the other biochemical results, although diarrhoea may be contributory. It may also be due to acidic metabolites of imidacloprid such as 6chloronicotinic acid and other metabolites; however,Imidazole metabolic pathways of imidacloprid have not been extensively studied in humans. Direct mitochondrial toxicity from a component of the formulation may cause anaerobic metabolism and produce a lactic acidosis which may cause a moderate decrease in bicarbonate. In animals, imidacloprid penetrates the blood-brain barrier to only a very limited extent. While a decreased level of consciousness was uncommon in our study, prolonged sedation and respiratory depression was noted in two patients which may have been due to co-ingestion of ethanol. Transient respiratory impairment appeared to contribute to deaths reported in patients with severe poisoning where co-ingestion of ethanol was not reported. There are no specific antidotes for neonicotinoid poisoning in mammals. On the basis of our experience, symptomatic and supportive care is all that is required for the management of patients with acute imidacloprid poisoning. Treatment with oximes such as pralidoxime is expected to be either ineffective or contraindicated. Oximes in the absence of organophosphorus pesticides have a weak inhibitory effect on acetylcholinesterase activity and therefore might increase nicotinic effects. It is notable that our two most seriously poisoned cases received treatment with pralidoxime. The concentration-time profile shown in Figure 3 suggests that there is rapid absorption, with high concentrations being noted on admission. In rats,(-)-p-Bromotetramisole Oxalate imidacloprid is rapidly and almost completely absorbed from the gastrointestinal tract. The peak plasma concentration is observed within approximately 2.5 hours and is followed by a rapid disposition phase. However, in our patients the concentrations generally remained elevated for up to 10–15 hours post-ingestion, which might suggest saturation of one or more kinetic pathways in humans at high doses. A possible factor influencing the observed kinetic profile is the administration of atropine which is known to prolong the absorption phase of xenobiotics.